Computed electroencephalographic activity mapping in schizophrenia. The resting state reconsidered.

Early diagnosis of dementia can be difficult. Quantitative EEG (qEEG) in combination with cognitive tasks shows promise for improving diagnostic accuracy. The study of task induced qEEG changes in normal ageing is a prerequisite for differentiating these changes from those which are specific to dementia. Sixteen young adults (mean age 28.8 ± 5.6 years) and 16 healthy cognitively normal older subjects (mean age 73.4 ± 7.9 years) participated in the study. EEG recordings were made while subjects were in a relaxed (or resting) state, and also while they performed arithmetic and language tasks. From the resting to the arithmetic conditions, there was decreased alpha activity and increased delta and beta-3 activity for both subject groups. Changes in alpha and delta activity were found in almost all sites and could be associated with arousal. Increase in beta-3 activity was focal, appearing only in the posterior region of the brain and it could be assumed that this area is highly involved in arithmetic processes. In the young adult group, theta activity increased from the resting to the arithmetic conditions, while in the older group theta activity changes were in the opposite direction. From the resting to the language condition, there was increased delta activity and decreased alpha and beta-1 activity for both subject groups. Changes in alpha and delta activity were again found in almost all sites. The decrease in beta-1 activity was found in only four sites, but these were not specific to a region of the brain known to be involved in language processing. This consistency in qEEG changes during cognitive tasks suggests that the method can be applied to the investigation of cognitive deficits associated with a number of neurological syndromes.

The aim of this study was to investigate topographic changes in electroencephalographic (EEG) power and frequency induced by abdominal surgery during anesthesia with 0.6% or 1.2% isoflurane in 66% nitrous oxide. Forty-six patients (aged 41 +/- 13 yr) scheduled for elective abdominal surgery were studied. The trachea of each patient was intubated and the lungs ventilated. Patients were randomly assigned to one of four groups: anesthesia was maintained with 0.6% (group 1, n = 12; group 2, n = 11) or 1.2% end-tidal isoflurane (group 3, n = 12; group 4, n = 11) in 66% nitrous oxide. Data were recorded over 20 min. Groups 1 and 3 were studied without surgery (as controls). In groups 2 and 4 recording was started 6 min before skin incision. The EEG was acquired via 17 scalp electrodes placed in standard International 10-20 locations (reference Cz). Absolute and relative power densities were calculated in selected frequency bands. EEG maps of spectral power densities were coded according to a continuous color spectrum. During baseline recordings, alpha activity was dominant at frontal areas in groups 1 and 2. In comparison, in groups 3 and 4, delta and theta activities were dominant at frontal leads. In group 2, the start of surgery resulted in increases in delta activity and decreases in alpha activity that were most dominant frontally (delta +181% and alpha -61%, F3). The delta shift was attenuated at 1.2% isoflurane (group 4, delta +44%, F3), but decreases in alpha activity (-53%, F3) were comparable to those in group 2. The EEG response in all frequency bands was attenuated at parietotemporal recording sites at both isoflurane concentrations. The current data demonstrate graded EEG responses induced by abdominal surgery during anesthesia with 0.6% or 1.2% isoflurane in 66% nitrous oxide. Spatial heterogeneities in absolute spectral power densities were reflected by color changes in the EEG maps. The topographic EEG analysis indicates that these changes were most dominant at frontal areas. The increases in delta and decreases in alpha activities may be related to intraoperative "paradoxical" electrophysiologic arousal phenomena.

To investigate the pathophysiology of narcoleptic patients' sleep in detail, we analysed and compared the whole-night polysomnograms of narcoleptic patients and normal human subjects. Eight drug-naive narcoleptic patients and eight age-matched normal volunteers underwent polysomnography (PSG) on two consecutive nights. In addition to conventional visual scoring of the polysomnograms, rapid eye movement (REM)-density and electroencephalograph (EEG) power spectra analyses were also performed. Sleep onset REM periods and fragmented nocturnal sleep were observed as expected in our narcoleptic patients. In the narcoleptic patients, REM period duration across the night did not show the significant increasing trend that is usually observed in normal subjects. In all narcoleptic patient REM periods, eye movement densities were significantly increased. The power spectra of narcoleptic REM sleep significantly increased between 0.3 and 0.9 Hz and decreased between 1.0 and 5.4 Hz. Further analysis revealed that non-rapid eye movement (NREM) period duration and the declining trend of delta power density in the narcoleptic patients were not significantly different from the normal subjects. Compared with normal subjects, the power spectra of narcoleptic NREM sleep increased in the 1.0-1.4 Hz and 11.0-11.9 Hz frequency bands, and decreased in a 24.0-26.9 Hz frequency band. Thus, increased EEG delta and decreased beta power densities were commonly observed in both the NREM and REM sleep of the narcoleptic patients, although the decrease in beta power during REM sleep was not statistically significant. Our visual analysis revealed fragmented nocturnal sleep and increased phasic REM components in the narcoleptic patients, which suggest the disturbance of sleep maintenance mechanism(s) and excessive effects of the mechanism(s) underlying eye movement activities during REM sleep in narcolepsy. Spectral analysis revealed significant increases in delta components and decreases in beta components, which suggest decreased activity in central arousal mechanisms. These characteristics lead us to hypothesize that two countervailing mechanisms underlie narcoleptic sleep pathology.

Replication of a P50 auditory gating deficit in Australian patients with schizophrenia

In this study a potential known as the contingent negative variation was used to differentiate between schizophrenic, Parkinson's disease (PD), Huntington's disease (HD) patients and normal control subjects. The aim was to assist diagnosis and the avoidance of false diagnosis. 20 schizophrenic, 16 PD, 11 HD and 43 normal control subjects were enrolled for this study. The discriminatory variables were generated by applying spectral analysis to pre- and post-stimulus sections of the CNV responses. The patient differentiation was achieved by using the measured variables in a discriminant analysis program. It was possible to accurately differentiate between HD, schizophrenic, PD patients and normal control subjects. It was also attempted to differentiate between HD and schizophrenic patients, HD and PD patients, and schizophrenic and PD patients. The test results indicated that the method is useful in differentiating between these patients. This study had a number of limitations. It was based on a limited number of individuals, and an analysis of medication effects on the test results and the test-retest reliability assessment could not be carried out.

Spontaneous oscillations of cerebral blood flow velocity in the middle cerebral arteries of normal subjects and schizophrenic patients

Location specific sleep spindle activity in the early visual areas and perceptual learning

Élaboration d’un questionnaire sur les cognitions alimentaires

Research has suggested the presence of brain damage as a cause or concomitant of chronic schizophrenia. The most recent research in this area has been the identification of abnormalities in schizophrenia by computed tomographic (CT) scans. A study was done to investigate localized changes in CT scan density numbers in the brains of schizophrenic patients, as opposed to the brains in normal control subjects. Twenty-four normal subjects and 23 schizophrenic patients were tested with CT scans. Density measurements in each area of the brain (left, right, anterior and posterior) were compared to three separate CT scan levels. Of six measurements of anterior left-hemisphere density, it was found that five showed lower density in schizophrenic brains, as compared with normal brains. Of the remaining 18 measurements that evaluated other areas of the brain, only three differentiated between schizophrenic patients and normal subjects. The results support the hypothesis that there are primary structural deficits in some schizophrenic patients, and these deficits are centered in and around the anterior area of the left (dominant) hemisphere. The results also demonstrated further implications.

It has been suggested that the positive symptoms of schizophrenic patients (hallucinations, delusions, and passivity experience) are caused by dysfunction of their internal and external sensory prediction errors. This is often discussed as related to dysfunction of the forward model that executes self-monitoring. Several reports have suggested that dysfunction of the forward model in schizophrenia causes misattributions of self-generated thoughts and actions to external sources. There is some evidence that the forward model can be measured using the electroencephalography (EEG) and magnetoencephalography (MEG) components such as N1 (m) and mismatch negativity (MMN) (m). The objective in this MEG study is to investigate differences in the N1m and MMNm-like activity generated in motor-auditory cross-modal tasks in normal control (NC) subjects and schizophrenic (SC) patients, and compared that activity with N1m and MMNm in the auditory unimodal task. The N1m and MMNm/MMNm-like activity were recorded in 15 SC patients and 12 matched NC subjects. The N1m-attenuation effects and peak amplitude of MMNm/MMNm-like activity of the NC and SC groups were compared. Additionally, correlations between MEG measures (N1m suppression rate, MMNm, and MMNm-like activity) and clinical variables (Positive and Negative Syndrome Scale (PANSS) scores and antipsychotic drug (APD) dosages) in SC patients were investigated. It was found that (i) there was no significant difference in N1m-attenuation for the NC and SC groups, and that (ii) MMNm in the unimodal task in the SC group was significantly smaller than that in the NC group. Further, the MMNm-like activity in the cross-modal task was smaller than that of the MMNm in the unimodal task in the NC group, but there was no significant difference in the SC group. The PANSS positive symptoms and general psychopathology score were moderately negatively correlated with the amplitudes of the MMNm-like activity, and the APD dosage was moderately negatively correlated with the N1m suppression rate. However, none of these correlations reached statistical significance. The findings suggest that schizophrenic patients perform altered predictive processes differently from healthy subjects in latencies reflecting MMNm, depending on whether they are under forward model generation or not. This may support the hypothesis that schizophrenic patients tend to misattribute their inner experience to external agents, thus leading to the characteristic schizophrenia symptoms.

Background Stroke is a leading cause of death and disability worldwide. In addition cognitive impairment (and dementia) and depression are common sequelae. Additional assessment methods which would better inform early prognostication of these unfavourable outcomes would engender substantial clinical benefits. For example, more accurate prognostication would enhance clinical decisions regarding appropriate levels of rehabilitation or care. This thesis investigates the potential utility, in this context, of one such assessment methodology; quantitative EEG (QEEG), performed in the first days after stroke. Study 1 (Chapter 2) The primary aim was to investigate the relationship between post-stroke QEEG measures and cognitive outcomes. Resting-state EEG was recorded within 62–101h after onset of middle cerebral artery (MCA) territory, ischaemic stroke. QEEG indices sensitive to power of one or more frequency bands were computed. The functional independence measure and functional assessment measure (FIM–FAM) was administered at approximately 3-months post-stroke. Total (30 items) and cognition-specific (5 items) FIM–FAM scores were correlated with QEEG indices using Spearman's coefficient. Twenty cases (10 female; age range 38–84) were analysed. Two QEEG indices demonstrated highly-significant correlations with cognitive outcomes: relative alpha power across the scalp (ρ=0.67, p≤0.001) and frontal delta/alpha power ratio (ρ=−0.664, p≤0.001). These results demonstrate that QEEG measures are associated with cognitive outcomes, and may potentially inform prognostication of same. Study 2 (Chapter 3) The primary aim was to investigate the ability of QEEG indices to inform prognostication of cognitive outcomes, assessed using the Montreal Cognitive Assessment (MoCA). Resting-state EEG was recorded within 48-239h after stroke symptom onset. Various QEEG indices analysed across the scalp were calculated. The MoCA was administered at approximately 3-months post-stroke and scores correlated with QEEG indices using Spearman's coefficient. Binary logistic regression was employed, with cognitive impairment indicated by MoCA scores ≤25. Thirty-one participants (10 female, age range: 18-84) were included in the analyses. Two measures of alpha frequency slowing (relative power in the traditional upper theta frequency range in posterior regions and peak alpha frequency across frontal and posterior regions of the scalp) were significantly positively correlated with lower MoCA scores. Using regression analysis, relative power of slowed alpha activity from 2 posterior regions were selected as optimal predictors of cognitive impairment. The regression model utilising these QEEG measures was able to accurately prognosticate cognitive impairment outcomes in 81% of the participants (25/31). These results indicate that the power of slowed alpha activity, acquired within several days of stroke onset from several electrodes only, can inform early prognostication of post-stroke cognitive outcomes. This QEEG measure would be of clinical value given the substantial numbers of stroke patients whom are unable to complete cognitive assessments, such as the MoCA, prior to hospital discharge due to functional impairments (as was the case in 13% of the patients recruited in the study). Study 3 (Chapter 4) The aim of the final study was to investigate potential associations between pre-discharge QEEG indices and post-stroke depression (PSD) outcome measures as well as the ability of QEEG to inform prognostication of PSD. (Methodology is detailed in Study 2, above). Outcome was assessed using the Geriatric Depression Scale (GDS) at approximately 3-months post-stroke. GDS scores were correlated with QEEG indices using Spearman's coefficient. Binary logistic regression was used to build a QEEG model to classify depression, indicated by GDS scores ≤6 (out of 15). A significant correlation was obtained between PSD and an index of interhemispheric asymmetry of delta activity, patients with more symmetric delta activity tended to have higher GDS scores (r=-0.475, p=0.007, n=31). This variable was entered into the binary logistic regression model, however, it was not found to be a statistically significant predictor of subsequent PSD. Conclusions The results of the studies reported in Chapters 2 and 3 collectively indicate that QEEG markers sensitive to alpha activity – particularly alpha slowing – following ischaemic stroke can inform early prognoses regarding post-stroke cognitive impairment. Notably, pre-discharge measures of slowed alpha activity, from several electrodes only, was found to reliably predict cognitive outcomes in the majority of patients investigated. Importantly, virtually all patients can be assessed with EEG, including the substantial proportion of patients who cannot be assessed with more routine assessment scales such as the MoCA; hence QEEG would be of particular clinical value in such cases. It is postulated that the observed associations between post-stroke measures of alpha slowing and cognitive outcomes are reflective of attentional function which appears linked to both variables. These novel findings and interpretations constitute the principal contributions of this thesis to the knowledge base in this field. In summary this research has considerable potential to ultimately contribute towards enhanced care and benefits for stroke patients and the broader community.

Alzheimer’s disease (AD) is a common neurodegenerative disease. APOE is the strong genetic risk factor of AD. The existing genome-wide association studies have identified many single nucleotide polymorphisms (SNPs) with minor effects on AD risk and the polygenic risk score (PRS) is presented to combine the effect of these SNPs. On the other hand, the volumes of various brain regions in AD patients have significant changes compared to that in normal individuals. Ch4 brain region containing at least 90% cholinergic neurons is the most extensive and conspicuous in the basal forebrain. Here, we investigated the relationship between the combined effect of AD-associated SNPs and Ch4 volume using the PRS approach. Our results showed that Ch4 volume in AD patients is significantly different from that in normal control subjects (p-value < 2.2 × 10−16). AD PRS, is not associated with the Ch4 volume in AD patients, excluding the APOE region (p-value = 0.264) and including the APOE region (p-value = 0.213). However, AD best-fit PRS, excluding the APOE region, is associated with Ch4 volume in normal control subjects (p-value = 0.015). AD PRS based on 8070 SNPs could explain 3.35% variance of Ch4 volume. In addition, the p-value of AD PRS model in normal control subjects, including the APOE region, is 0.006. AD PRS based on 8079 SNPs could explain 4.23% variance of Ch4 volume. In conclusion, PRS based on AD-associated SNPs is significantly related to Ch4 volume in normal subjects but not in patients.

BackgroundHighly structured electroencephalography (EEG) oscillations can occur in adults during etomidate-induced general anesthesia, but the link between these two phenomena is poorly understood. Therefore, in the present study, we investigated the electroencephalogram dynamics of etomidate-induced loss of consciousness (LOC) in order to understand the neurological mechanism of etomidate-induced LOC.MethodsThis study is a prospective observational study. Etomidate-induced anesthesia was performed on eligible patients undergoing elective surgery. We analyzed EEG data from 20 patients who received etomidate for the induction of general anesthesia. We used power spectra and coherence methods to process and analyze the EEG data. Our study was based on 4-channel EEG recordings.ResultsCompared with the baseline (awake period), etomidate induced an increase in power in delta, theta, alpha and beta waves during LOC. Compared with the awake period, the delta-wave (1–4 Hz), alpha-wave(8–13 Hz), and theta-wave(4–8 Hz) coherence increased significantly during LOC, while the slow-wave (< 1 Hz) coherence decreased. However, the delta wave (1.0–4.0 Hz) during etomidate-induced LOC was more coherent than during the awake period (1.86–3.17 Hz, two-group test for coherence, p < 0.001).ConclusionsThe neural circuit mechanism of etomidate-induced LOC is closely related to the induction of oscillation in delta, theta, alpha and beta waves and the enhancement of delta-wave coherence.Trial registrationChiCTR1800017110

V4. Focal slow wave in patients after epilepsy surgery with and without seizure recurrence

Carpal tunnel syndrome (CTS) is one of the most common upper limb compression neuropathies. CTS account for approximately 90% of all entrapment neuropathies. An estimated one million adults from the United States (annually) have CTS requiring medical treatment. The aim of the study is to investigate to compare the normal values of median nerve of normal healthy women (distal latency, amplitude &amp; conduction velocity) with the same values of median nerve in women with carpel tunnel syndrome. The study was conducted as a case series study for Iraqi volunteers and patients attended to rheumatology department - neurophysiology unit at Tikrit teaching hospital (TTH) at the period from the 1st of December 2010 to the 1st of August 2011. Forty healthy female subjects with a mean age of (40.315 ± 10.324 years) to compare with the CTS female patients. Thirty eight female patients with mean age group of (40.55 ± 10.230 years) with CTS affect them in right hand diagnosed by rheumatologist and neurologist then referred to nerve conductive study (NCS) and EMG unit at TTH. The NCS was done by using NIHON KOHDEN / Neuropack S1 EMG / EP Measuring System MEB-9400 MODEL 2009. There are no significance differences between control subjects &amp; CTS patients regarding age, body mass index. Also, there are no significance difference between normal control subjects &amp; CTS patients in regard to upper limb length, arm circumference, index finger length (IFL), index finger circumference and wrist circumference. In regard to motor activity of median nerve, there is significance increase in distal latency time of median nerve of CTS patients (5.632 ± 1.791 msec) on compare to normal control subjects (3.540 ± 0.622 msec). Also, the amplitude of action potential of motor activity of median nerve is higher in control subjects (9.217 ± 0.509 mv) in compare to CTS patients motor activity of amplitude of (6.530 ± 1.937 mv). The difference between median nerve motor amplitude is significance at ( p&lt;0.01) between patients and controls. Moreover the conduction velocity in CTS patients of median motor (58.354 ± 1.789 m/sec) is significance lower (p&lt;0.01) in compare to motor conduction values of median nerve in normal control subjects (53.744 ± 4.232 m/sec). However, in regard to sensory activity of median nerve in right hand of both normal control subjects and CTS patients. The latency period in CTS patients is delayed (3.414 ± 1.606 msec) in compare to normal subjects (2.761 ± 0.344 msec). While, the amplitude of action potential of the sensory activity of median nerve is significantly lower (p&lt; 0.01) in compare to normal subjects. Also, the conduction velocity of sensory activity of median nerve of CTS patients is significantly lower (38.357 ± 4.357 m/sec) on compare to conduction velocity of sensory activity of median nerve of normal subjects (48.236 ± 2.545 m/sec). The present study concludes that: The present study showed abnormal values NCS of median nerve at CTS patients as compare to normal healthy women of same age. The present study recommend that;- Using median nerve ultrasonography as diagnostic tools to confirm or exclude CTS &amp; minimize false positive results.